Coumadin -- Yes or No?

Since I was diagnosed with lone A-fib in July, I've seen cardiologists and electrophysiologists at two different centers, one in Boise, Idaho, where my wife and I have a second home, and last week at the Cleveland Clinic Foundation, which I visited by driving 7 hours from my Illiinois home.

In Idaho, I was started on Coumadin.

At CCF, I was told I do not need to be on Coumadin.

Well, if you see ten different doctors, you may get ten different opinions. But I am interested in whether others who populate this bulletin board have had similar experiences.

A little background on my case may be in order:

I am a 62-year-old male and have absolutely no other risk factors for stroke, other than being an A-fib sufferer. At CCF, the cardiologist I saw, Dr. David Martin, said current American College of Cardiology guidelines recommend Coumadin only after age 75 (yes, 75, not 65) for patients like me, i.e. LAF with no stroke risk factors.

Instead of Coumadin, the recommendation is for 375 mg of aspirin daily, for my profile, I was told.

I have not spoken yet to my Idaho cardiologist about this contradiction. I suppose he was being ultra-conservative. Persons who do have other risk factors for stroke are started on Coumadin at age 65, rather than 75, and I remember him saying that "We haven't had such good results with aspirin."

The advice I got at CCF was good news to me, since I went there to ask about getting off Coumadin, though I expected to be told the only hope of escaping Coumadin was to have an ablation. I was told I could go ahead with an ablation if I wanted, but that since I tolerate my A-fib episodes (which encompass about 30% of my time) well, I ought to consider waiting two or three or more years, because methods, tools and techniques will have improved significantly by then.

Enough for now on this, but any accounts of experiences relevant to mine would be appreciated.

Thanks to all in advance,

JP

JP,

The rule of thumb is if you are out of NSR for 48 hours or more at a stretch, you should consider coumadin. If you are in NSR for several hours each day, you probably don't need it.

Idaho was right about one thing. Study after study has shown aspirin does not work as well as coumadin. And I have heard (Dr. Stephen Sinatra) that as many as 10,000 people in the U.S. die due to bleeding caused by aspirin. Another study (released yesterday) said regular, prolonged use of aspirin can increase the chances of pancreatic cancer in women.

Nevertheless, until I started being in flutter most of the time, I took a baby aspirin a day. Now, I am on coumadin - at least until I have an ablation, probably next month.

BillB
48;A;2000

Thanks, Bill, for your experience with aspirin vs. Coumadin. My LAF spells seldom last as long as 48 hours -- 24 to 36 hours is more the norm for me. But I once had an episode that lasted for four and a half days. I think that event played a role in prompting my Idaho cardiologist to put me on Coumadin.

I plan to stay on Coumadin for the time being, but when I undertake activities that put me far, far from a modern hospital, such as an extended trip in the Himalayas, I plan to quit the Coumadin before departing and resume it on return. Ditto for mountaineering expeditions, which I participate in at least once a year.

JP

This is the best explanation i have read so far as to why coumadin is more effective than plavix and aspirin-jerry



(by Dr. Moll, Thrombophilia Program, Center for Thrombosis and Hemostasis, UNC Chapel Hill, N.C., USA). ________________________________________
35. Aspirin, Plavix, and Coumadin®; - when to use what
Q1: "What is the difference between using coumadin® and Plavix for treating clotting disorders? Do you need to be tested for your INR with Plavix ? If not, why do so many of us get placed on coumadin® instead of Plavix ? Is Plavix also influenced by vitamin K food intake?"
A1: Plavix , similar to aspirin, is effective in treating arterial clots (stroke, heart attack, peripheral arterial disease), whereas coumadin® is effective in treating venous clots (deep vein thrombosis or pulmonary embolism). Plavix does not influence the INR. Plavix' action is not influenced by vitamin K intake.

Q2: "I don't really understand the issue about aspirin helping prevent arterial clotting but not venous clots. Can anyone shed any light?"
A2: When we injure ourselves and bleed, the normal function of platelets is to clog up the hole in the blood vessels. Platelets do that by sticking together and forming a platelet plug. Medications such as aspirin, plavix® , ticlid® , and aggrenox® impair platelet function, so that platelets do not stick together as well. In laymen's terms this is called making "platelets less sticky"; in medical terms this is called "inhibiting platelet aggregation". The effect is, that people do not clot as easily. This effect is mainly seen in arteries (see explanation below).

Q3: "My mother called today and said she's been diagnosed with fibromuscular dysplasia. The medication they placed her on was Plavix® . I was wondering why they didn't put her on coumadin®."
A3: Fibromuscular dysplasia is an uncommon disorder, in which for mostly unknown reasons blood vessel walls thicken and thereby narrow their opening (= lumen). Since it is mainly an arterial problem, anti-platelet drugs, such as Aspirin or Plavix® , are the medications of choice.

Q4: "Does Aspirin therapy help prevent deep vein thrombosis?"
A4: In most cases probably not.

When we injure ourselves and bleed, platelets clog up the hole in the blood vessels. Platelets do that by sticking together and forming a platelet plug (= platelet aggregation). The plug is then strengthened by our clotting factors, which form a meshwork consisting of fibrin. One can prevent the formation of blood clots by either impairing platelet function, or by decreasing the activity of the clotting factors and thereby the fibrin-meshwork formation.

Arteries are thick blood vessels with fast flowing blood. Blood clots in arteries are typically triggered by underlying roughening of the artery wall (= arteriosclerosis; atherosclerosis); blood platelets get stuck to the roughened blood vessel wall and form a clot. Thus, the medication of choice in trying to prevent thrombosis in arteries (i.e. stroke, heart attack, peripheral arterial disease, retinal artery thrombosis, etc.), are medications that act against platelets. The following medications are anti-platelet drugs:
• Aspirin (= ASA)
• Plavix (= Clopidogrel)
• Ticlid (= Ticlopidine)
• Aggrenox (= aspirin plus dipyridamole)
By interfering with platelet function, these drugs increase the patient's risk of bleeding, even though to a lesser degree than coumadin . The INR is not influenced by these drugs. Vitamin K intake does not influence these drugs.

Veins are made up very differently than arteries. Veins are thin blood vessels with slow flowing blood. Blood clots that form in veins (deep vein thrombosis, pulmonary embolism, etc.) are mainly made up of clotting proteins; platelets do not play a big role in venous clots. Coumadin® (= warfarin) is an effective "blood thinner" by preventing the production of clotting factors in the liver, increasing the INR. It is therefore the drug of choice in venous thrombosis. Anti-platelet drugs do not play much of a role in preventing venous clots.

Occasionally, clots in arteries originate from one of the two left heart chambers (= left atrium, left ventricle) and travel from there with the blood stream to the brain, the retina, or the extremities. This typically happens in atrial fibrillation (= irregular heart beat). Such a clot is called an arterial embolism (= arterial thromboembolism; plural: "emboli"). These arterial emboli resemble the type of clots seen in veins, i.e. they have little platelet participation. They are therefore best treated with coumadin® , not with anti-platelet drugs, even though they are clots in arteries.

Additional comment from Dr. Moll: If a patient with venous blood clots comes off coumadin® and asks whether he/she should take aspirin to prevent further clots I usually tell him/her that aspirin is unlikely going to prevent any venous clots

[www.fvleiden.org]

I certainly feel more secure taking it than I would be regular aspirin. In fact, during one ER visit the ER doctor gave me 2 baby aspirins knowing I was on Coumadin, I asked why........answer: works on different platelets of the blood. Who knew?

JP - Hans posted an explanation a while back on why Coumadin vs. aspirin... perhaps he will re-post it.

Coumadin works on one clotting mechanism; aspirin - another.

Hans?


Jackie

Jerry, thanks so much for posting the Q&A regarding aspirin and other "anti-platelet" drugs vs. Coumadin. It really lays out the differences.

Hans' book, "Lone Atrial Fibrillation: Towards A Cure," explains the differences, too, on pages 122-4, with a good discussion of pros and cons and a list of the general guidelines for prescribing aspirin vs. Coumadin.

I had not read this material when I posted my original message at the top of this string.

Thanks to all for the discussion.

JP

Jerry - much thanks for that explanation.

About 2 years ago when I had a consulation with one of the top EP's at the Clinic, it was recommended that I stay on Coumadin at least 6 months after being in NSR. Now, if I understand correctly, patients are suppossed to be able to stop 3 months after a pulmonary vein ablation. BUT, does that mean only if you are in NSR at the time of the 3 month checkup? I'm not sure.

Since I'v been on it 4 1/2 years, I'm almost afraid to go off of it immediately after my 3 month checkup.

njb

Hi NBJ,

How have you been? Have you had any success is getting answers/help from CCF? Or are you still "in the ring" like many of us fighting for information and answers?

I see Dr. Natale next Wednesday. 2 weeks ago I had my follow up visit with my EP. In reviewing all of the information from the 30 day event monitor and the holter monitor, along with the problems I'm currently experiencing, he told me I basically have 2 options. First, I could do drug therapy for 5 years while ablation technology continues to improve, or I could have another ablation. I'm very anti meds so I've scheduled the ablation for 12/19 (flutter ablation and attempt to target foci causing so many problematic PACs). In the meantime, I'm going to see Dr. Natale for another opinion. It'll be very interesting to see what happens.

I hope you're making progress. In answer to your post, I highly recommend the event monitor. It's attached all the time and I was able to "take" 2 events before having to transmit. Sometimes I was transmitting quite a few times a day, other times only 1-3 times during quieter days. My only problem with the event monitor is that I'm allergic to the adhesive on the pads (even the "infant" type that are not supposed to cause skin reactions) and after the 3rd week, I had to stop wearing the monitor because I'd developed rashes, blisters, and a hypersensitivity to the patches. Therefore, I only attached the pad and leads, took reading, and transmitted when my events were particularly bothersome. The information the 30 day event monitor captured was very interesting and certainly great information for my EP in reviewing my status and recommending further treatment.

Take care and keep in touch.